A 1300-year multi-proxy, high-resolution record from a rich fen in northern Poland:Reconstructing hydrology, land use and climate change

Here we present the first high-resolution multi-proxy analysis of a rich fen in the central-eastern European lowlands. The fen is located in the young glacial landscape of the Sta{ogonek}zki river valley. We investigated the fen's development pathways, asking three main questions: (i) what was the pattern and timing of the peatland's vegetation succession, (ii) how did land use and climate affect the succession in the fen ecosystem, and (iii) to what degree does the reconstructed hydrology for this site correlate with those of other sites in the region in terms of past climate change? Several stages of fen history were determined, beginning with the lake-to-fen transition ca. AD 700. Brown mosses dominated the sampling site from this period to the present. No human impact was found to have occurred until ca. AD 1700, when the first forest cutting began. Around AD 1890 a more significant disturbance took place-this date marks the clear cutting of forests and dramatic landscape openness. Deforestation changed the hydrology and chemistry of the mire, which was revealed by a shift in local plant and testate amoebae communities. We also compared a potential climatic signal recorded in the peat profile before AD 1700 with other sites from the region. © 2013 John Wiley & Sons, Ltd.

Carbachol triggers RyR-dependent Ca(2+) release via activation of IP(3) receptors in isolated rat gastric myocytes.

Possible interactions between different intracellular Ca(2+) release channels were studied in isolated rat gastric myocytes using agonist-evoked Ca(2+) signals. Spontaneous, local Ca(2+) transients were observed in fluo-4-loaded cells with linescan confocal imaging. These were blocked by ryanodine (100 microM) but not by the inositol 1,4,5-trisphosphate receptor (IP(3)R) blocker, 2-aminoethoxydiphenyl borate (100 microM), identifying them as Ca(2+) sparks. Caffeine (10 mM) and carbachol (10 microM) initiated Ca(2+) release at sites which co-localized with each other and with any Ca(2+) spark sites. In fura-2-loaded cells extracellular 2-aminoethoxydiphenyl borate and intracellular heparin (5 mg ml(-1)) both inhibited the global cytoplasmic [Ca(2+)] transient evoked by carbachol, confirming that it was IP(3)R-dependent. 2-Aminoethoxydiphenyl borate and heparin also increased the response to caffeine. This probably reflected an increased Ca(2+) store content since 2-aminoethoxydiphenyl borate more than doubled the amplitude of transients evoked by ionomycin. Ryanodine completely abolished carbachol and caffeine responses but only reduced ionomycin transients by 30 %, suggesting that blockade of carbachol transients by ryanodine was not simply due to store depletion. Double labelling of IP(3)Rs and RyRs demonstrated extensive overlap in their distribution. These results suggest that carbachol stimulates Ca(2+) release through co-operation between IP(3)Rs and RyRs, and implicate IP(3)Rs in the regulation of Ca(2+) store content.